The amendment to the Statement of Principles for malignant neoplasm of the prostate dated 9 December 1996 required dietary intake of 70g/day of animal fat for at least 20 years and that should have increased by 40% associated with a period of service in order for there to be a causal connection between that diet and the development of carcinoma of the prostate.

In relation to this I have been asked to provide input by determining if there is any evidence of a relationship between fat intake and addiction. In other words if fat over-consumption can be construed as an addiction.

There are three issues I will address in covering this overall question:

What are the psychological and psychophysiological processes that facilitate fat consumption?

Can fat over-consumption be viewed an addiction?

Is there a special case for binge eating disorder as an example of an addiction to food and more specifically to fat?

A number of caveats must be stated at the outset of this report.

a. Firstly almost all research into the psychophysiology of fat consumption does not differentiate the effects of animal from vegetable fat. Thus no definitive statement concerning animal fat consumption and addiction can be made.

b. Almost all research has evaluated the effects of combined fat and flavour, either sweet (sugar) in the majority of cases, or savoury (salt). Hence in many instances it is not possible to absolutely distinguish the factors associated with consumption of carbohydrates from those for fat.

c. In spite of this, the evidence on fat consumption can be validly considered if one views fat consumption in relation to fat foods: foods where the macronutrient content is primarily rather than, necessarily, exclusively fat.

1. What are the psychological and psychophysiological processes that facilitate fat consumption?

A. The sensory/hedonic characteristics of fat are pleasurable and reinforcing.

There are two “opponent” processes that influence food consumption, pre-ingestive, or sensory, and post-ingestive. Afferent or sensory information from ingested food acting in the mouth provides primarily positive feedback for eating. The stomach and small intestine provide primarily negative feedback to the process of consumption (Blundell & Hill, 1993). In rats where post-ingestive process is removed (sham-feeding) the sensory characteristics of fat alone influence intake, such that the intake of fat increases over time (Reed, et al, 1989). Hence in terms of sensation, fat consumption is reinforcing.

Blundell and Hill (1993) suggest that in humans the appeal of fat lies in the texture of fat and tastants embedded in the fat rather than the fat itself.

However there is some evidence to suggest that there are gender differences in the preferences for flavour-fat combinations. Pangborn, et al. (1985) found that women’s hedonic rating of the fat in milk or chocolate milk did not differ significantly according to fat intake or type of milk consumed. Laurent, de Matteis, Hofstetter, and Schultz (1994) found that at any age or weight, men preferred sweet fat food (as opposed to other fatty or non-fatty foods.)

Furthermore, learning may also be a factor in preference for fat. Bowen, et al (1992) found that subjects ate more ice-cream when they were told it was high-fat, compared with when they were told it was low-fat, irrespective of the actual fat content, suggesting that they had learnt that something high in fat will be more pleasurable.

B. The other or “opponent” side of the process of consumption of fat is the post-ingestive effect which appears to be aversive as a means of modulating fat consumption. This process is weakened through repeated exposure to high fat diet.

Rats used to a low fat diet when presented with high fat consume much less fat than rats used to a high-fat diet (Warwick, et al, 1990).

When rats used to a low-fat diet are put on a high-fat diet and then given a choice of high versus low-fat foods, they consume less fat than rats who were on a high-fat diet. (Warwick, et al, 1990)

Although rats fed on a no-fat control diet for 12 days had higher intake of fat-adulterated food when exposed to a choice paradigm initially, this intake of fat decreased significantly from Day 1 to Day 3. This suggests that although rats initially preferred the fatty food as they came off the restricted diet (probably due to hedonic/sensory factors) this preference very quickly decreased (probably because of aversive postingestive effects) (Naim, et al, 1987.)

In humans food preferences, including fat preferences, develop very early in life and are fairly resistant to change (Capaldi, 1996).

Therefore the preference for fat, and hence increased fat intake, should be increased in an individual if the reinforcement of the positive sensory impact of the fat is greater than the delayed aversive postingestive consequences of consuming fat. However the available evidence indicates that the aversiveness of post-ingestive process appears to be intrinsic, and, furthermore, is difficult to change once established. Similarly extended exposure to high fat can reduce the aversiveness of the post-ingestive process. Therefore in order to change fat preferences (and consumption), the positive sensory impact of the fat would need to be significantly enhanced to counteract the post-ingestive negative feedback. Alternatively, the aversiveness of the post-ingestive consequences of fat consumption would need to be reduced through repeated exposure, although there is no data available on how long a period this might need to be.

C. Information regarding the health-effects of fat can effect consumption and preference.

Whilst there is evidence that children and adolescents are resistant to information aimed at changing dietary preferences (Nowak & Speare, 1996; Capaldi, 1996) this is not so for adults.

Bowen, Tomoyasu, Anderson, Carney & Kristal, (1992) found education given about the link between diet and cancer found that it significantly decreased consumption of, and reported preference for, fat.

Thus information can effect fat preference and consumption. The implication being that conscious process and intention is involved in fat preference and consumption.

D. Three other factors have been shown to effect food preferences and consumption, but not fat specifically.

i. Caloric density.

Fat is a very dense caloric food (9 kcal/g versus 4 kcal/g for protein and carbohydrate.) Blundell and Hill (1993) suggest that due to its calorie density a large number of “fat” calories can be consumed very rapidly before the post-ingestive mechanisms can be brought into operation. The overall effect is one of passive over-consumption (Blundell, Lawton, Cotton, Macdiarmid, 1996).

Bolles, Hayward, & Crandall (1981) also found that caloric density is more important than number of calories in determining food preferences and consumption.

ii. Emotions

Emotions are viewed as important precursors of over-consumption of food (Kenardy, et al, 1996.) The impact of emotions can be either to suppress appetite (Stone & Brownell, 1994) or enhance it (Ganley, 1989).

iii. Variation of diet

Consumption of different foods can modify the level of satiation. For example after eating a food to fullness, if a food of another palatable flavour is introduced, there is a reduction of perceived fullness, and therefore increased consumption of the more recently presented food. This is sometimes called “the dessert effect” (Capaldi, 1996.)

2. Can fat over-consumption be viewed as substance dependence (or an addiction)?

If an underlying mechanism of addiction could be construed for over-consumption of fat, it might be possible to view over-consumption of fat for an extended period of time as due to an addiction to fat. For over-consumption of fat to be construed as an addiction, it would need to fit within the DSM-IV (APA,1994) diagnostic criteria for Substance Dependence. While Substance Dependence is a diagnostic category normally reserved for alcohol and drug addiction, fat could be defined as a substance. However there are a number of required features in order that fat over-consumption be defined as an addiction.

A maladaptive pattern of substance use, leading to clinically significant impairment or distress, as manifested by three (or more) of the following, occurring at any time in the same 12-month period:

Tolerance, either (a) a need for a markedly increased amounts of the substance to achieve intoxication or the desired effect, or (b) markedly diminished effect with continued use of the same amount of the substance.

Withdrawal, either (a) the characteristic withdrawal syndrome for the substance, or (b) the same or closely related substance is taken to relieve or avoid the withdrawal symptoms.

The substance is often taken in larger amounts or over a longer period than was intended

There is a persistent desire or unsuccessful efforts to cut down or control substance use

A great deal of time is spent in activities necessary to obtain the substance, use the substance, or recover from its effects

Important social, occupational, or recreational activities are given up or reduced because of substance use

The substance use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the substance (APA, 1994.)

A. Tolerance

The addiction model as applied to alcohol and psychoactive drugs explains tolerance through a process of anticipatory conditioned compensatory responses (CCRs). Specifically, body functions adjust to restore the homeostasis disrupted by the substance (eg lower the core body temperature to compensate for the rise in temperature produced by the consumption of alcohol). Through classical conditioning the body elicits these CCRs in an anticipatory fashion when an associated stimuli is present (eg taste, smell, environmental stimuli, even cognitions such as thinking about drinking). These compensatory responses lower the effect of the substance and thus increases the amount of the substance is needed to attain the desired effect (tolerance), [or if the associated stimuli are not followed by the intake of the substance withdrawal effects are felt.]

Jansen (1994) and others (Wilson, 1993; Woods & Brief, 1988) refer to “cephalic phase responses” which describes conditioned compensatory responses for eating. According to Jansen (1994) the over-consumption of carbohydrates leads to a bodily compensatory response of releasing more insulin into the blood. This assists in the absorption of glucose from the blood stream in order to regulate the blood-sugar level. This process is seen as evidence of a tolerance occurring to carbohydrates. However, there seems to be no evidence of an equivalent process for the regulation (and thus tolerance to) fat.

Both rats and humans (over)compensate for dilution or substitution of their regular fat intake suggesting that there is some kind of regulatory system for fat. However this system is not very precise, at least in comparison to that involved in the regulation of carbohydrate (insulin) and alcohol (thermoregulation) consumption. For example dilution of a fat diet causes a rebound over-consumption of up to 50% of baseline total fat intake (Blundell & Hill, 1993; Castonguay et al., 1994; Cotton, et al, 1996).

There is ample evidence that endogenous opioids (EO) play a role in manipulating the consumption of fat in rats (eg Shide & Blass, 1991; Yim & Lowy 1984). While this indicates a possible role of EOs as conditioned compensatory responses (CCR’s) in a “fat addiction”, for EO’s to have such a compensatory role in fat over consumption, there must be evidence of an effect of fat consumption on the levels of EO’s (as alcohol raises temperature, or carbohydrates increase the blood-sugar level). Only one study could be found that provides any evidence of food consumption effecting EO levels (Dum, Gramsch, & Hery, 1983). This study found that the binding of an injected peptide (3H-etorphine) in the hypothalamus of rats was significantly reduced after consumption of “highly palatable” solution. This was interpreted for a process where the solution have induced release of opioids. Unfortunately this highly palatable solution was likely to be a combination of fat and sugar. There is certainly evidence of “highly palatable” foods (rich in both fat and sugar) producing direct effects such as high plasma Beta-endorphin levels and analgesia , and indirect effects such as actual loss of morphine-induced analgesia (via induced opiate tolerance through EO release) (Cohen, et al 1984; Fullerton & Getto, 1985; Lieblich, et al 1983; McCloy & McCloy, 1979; Zhang, et al, 1994). However there is little evidence for the effect of fat alone (as opposed to fat combined with carbohydrates) on EOs. Thus support for a role of EOs as compensatory mechanisms for the regulation, and thus tolerance of fat consumption is not yet available.

B. Withdrawal

Le Magnen (1990) reports that rats fed a “cafeteria diet” (choice of highly palatable high energy foods) for three weeks show symptoms of piloerection, head and whole body shaking, teeth chattering and tremors (morphine-like withdrawal symptoms) when returned to “stock diet” (restricted choice of lower energy food.) Although this could be construed as evidence of “fat withdrawal”, the “cafeteria diet” is a highly palatable, high calorie diet, a mixture of both fat and carbohydrate. Again it is not possible to determine whether the withdrawal effects result from fat or high-energy carbohydrates (eg sugar.)

C. Loss of control (substance taken in larger amounts and over a longer time than was intended)

There is no evidence from the literature that a loss of control governs fat over-consumption. While it could be argued that the tendency for over-consumption of fat (Bludell & Hill, 1993) is an indication of fat -induced loss of control, this is most likely due to the high caloric density and slow post-ingestive feedback of fat intake, rather than an active over-consumption or loss of control.

Finally there is no evidence for fat over-consumption as meeting any of the last four criteria for DSM-IV Substance Dependence. Therefore there is little support for a “fat addiction” under the DSM-IV Substance Dependence criteria.

Summary

Consumption of fat is perceived as pleasurable, however this fat preference is 1. probably related to “tastants” embedded in the fat, rather than the fat itself; 2. subject to individual and group (gender) variation probably through associative learning; and 3. modifiable by new information. At a psychophysiological level fat preferences and consumption are effected by pre-ingestive sensory processes and post-ingestive processes. It is the dynamic balance between these two processes that determine actual consumption. Whilst it is possible to change this balance, it is probably fairly resistant to change, requiring significantly greater sensory valance at the pre-ingestive level, and/or a long term exposure to a new diet (eg high fat).

Overall, the evidence in favour of an addictive model of fat over-consumption is very limited and this is further supported by the “lack of fit” of over-consumption of fat under the Substance Dependence criteria defined by DSM-IV.

3. Is there special case for Binge Eating Disorder as a “fat addiction”?

Binge eating is the uncontrolled consumption of large amounts of food. As a behaviour it can be present in anorexia nervosa, is a defining feature of bulimia nervosa when it is also associated with compensatory behaviours such as voluntary vomiting, and is central to a new disorder, binge eating disorder. Binge eating disorder is included with the DSM-IV (APA, 1994) as requiring further research.

According to DSM-IV the definition of binge-eating involves two key aspects:

1. Loss of control during eating, that is a sense that one cannot stop eating or control what or how much one is eating;

2. Consumption of a relatively large amount of food over a relatively short period of time (about two hours).

Furthermore according to the DSM-IV binge eating disorder must also incorporate:

A. Bingeing at least twice weekly for the last six months;

B. Concern about bingeing and weight;

C. Three of the following during most binges:

i. Eating until feeling uncomfortably full.

ii. Eating large amounts of food when not feeling hungry.

iii. Eating large amounts of food throughout the day with out planned meal times.

iv. Eating alone because of being embarrassed.

v. Feeling disgusted depressed or guilty after overeating.

vi. Eating much more rapidly than usual.

D. No compensatory behaviours (APA, 1994.)

If fat were addictive then binge eating could be viewed as an expression of that addiction. Therefore evidence for binge eating as a special case of a “food addiction” will be examined as well as evidence of specific fat over-consumption within binge eating.

Is there a higher preference for fat in binge eating?

As stated above, binge eating is present in bulimia and anorexia nervosa, as well as binge eating disorder. Within bulimia and anorexia binges are usually part of a dietary restriction-binge cycle, whereas binges in binge eating disorder tend not that have significant dietary restriction interposed (APA, 1994; Wilson, 1993.)

During binges associated with bulimia nervosa and anorexia nervosa evidence indicates there is a higher consumption of fat (percentage of total calories consumed) but that this is seen to be a function of restriction of fat (van der Ster, et al, 1994; Kales, 1990; Tuschl et al, 1990; Woell et al, 1989.)

In contrast the limited studies of macronutrient intake during binge eating in binge eating disorder have mixed results regarding the consumption of fat in binges than Non-binge eating.

Rossiter et al (1992) examined obese binge-eaters took food records for a week. They found no difference in proportions of fat or carbohydrate intake between binge episodes and non-binge days, but protein and fibre intake were higher on non-binge days.

Yanovski et al (1992) found that bingers compared to non-bingers were instructed to eat a normal meal there was no difference in macronutrient composition, although under both conditions the binge eater consumed significantly more calories

Both studies indicate that total calorie intake is increased by, on average, 50% in the diets of patients with binge eating disorder versus non-patient controls.

How well does binge eating disorder fit into Substance Dependence criteria?

As with fat over-consumption, binge eating disorder can also be examined in relation to the Substance Dependence Criteria of DSM-IV.

Tolerance

Cephalic Phase Responses (Jansen, 1994) have been hypothesised the CCR’s within eating disorders. However as stated previously Cephalic Phase Responses have only been linked to carbohydrates. Furthermore a study by Karhunen, et al. (1997) showed no stronger cephalic phase response in obese binge-eaters than obese non-binge-eaters, after examining serum insulin, free fatty acid and plasma glucose concentrations; and salivation, feelings of hunger and desire to eat. Bingers did, however report a greater desire to eat during food exposure than did the non-bingers. This suggests that binge eating may be more motivationally rather than physiologically controlled and therefore argues against a “tolerance” process.

Furthermore overcoming tolerance in the case of binge eating disorder is different from the addiction model of alcohol and other psychoactive drugs, in that for these substances abstinence is required for recovery; but for binge eating the goal is to regulate meals and macronutrient intake (Gendall, et al. 1997; Goodrick & Foreyt 1991).

Withdrawal

Similar arguments can be applied to withdrawal as to tolerance. For example Jansen (1994) proposed that CCRs tend to experienced as “craving” or withdrawal from the substance. Further, binge eating exaggerates the hypoglycaemic (craving) response because the conditioning is stronger when the intake of the substance is huge (rendering the body hypoglycaemic if the substance is not consumed).

The substance is often taken in larger amounts or over a longer period than was intended

The defining characteristics of binge eating are encompassed within this criterion, that is loss of control of consumption and over-consumption.

Marcus (1993) reported that obese binge-eater (compared to obese non-binge eaters) had significantly less perceived control over eating; and they were more preoccupied with thoughts of food, and impulses to overeat.

There is a persistent desire or unsuccessful efforts to cut down or control substance use.

While there is evidence in bulimic patients that they restrict their diets in response to episodes of binge eating, in obese binge eaters, compared to obese non-binge eaters there is less of a tendency to apply specific strategies to control consumption. However there is typically a long history of repeated unsuccessful efforts to control food intake (APA, 1994)

There is no evidence to support binge eating disorder as meeting the last three criteria for substance dependence.

In summary, there is some evidence that Binge Eating Disorder could be construed as an addiction. However, the level and amount of this evidence is not conclusive.

Is Binge Eating Disorder a possible mechanism for the Statement of Principles Criterion for fat over-consumption as a cause of Prostate Cancer?

Binge Eating Disorder could possibly be considered as an addiction, but the evidence is not conclusive.

If certain assumptions are made based on the literature then it could be argued that a person who engaged in binge eating on a daily basis for 20 years would probably exceed the 70 g animal fat consumption required for the dietary fat intake criterion in the Statement of Principles.

The following assumptions are required for this conclusion to be supported:

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